Some previous lecturers in this series have recounted their lifes work; others

have given challenging philosophical perspectives. I do not intend this

presentation should be just a stroll down memory lane, though I may call upon
some of my own experiences in developing the point of my message. Rather, in
the light of my career as a poultry nutritionist, I want to convey the importance
of the contribution of nutritional understanding and research to poultry science
and production, taking past and present experiences as examples and to
discuss areas where new knowledge is still required and where new
opportunities may arise. In particular, I wish to highlight the importance of
the interaction of nutrition with other disciplines, and how nutrition can have an
impact in so many areas. Vence te titule of mi lectura.
In considering the content of my talk, I have recalled the challenging views put
forward by Trevor
Morris (1989 ) at the Turkey Science Symposium, where his message was
essentially that we knew enough then about nutrition (bar a few erratics) to
feed poultry. If we knew the genetic potentials of birds, then with appropriate
models we could predict how much energy and amino acids to feed them to
optimize performance and if we provided sufficient quantities of vitamins, we
could rule out deficiency problems. He was talking about turkeys but the
implication was general.
If we take a rather narrow view of nutrition under model conditions with
minimal economic pressures, there may be some truth in this view. Indeed,
there are computer-based feeding systems that make a good job of supplying
nutrients to birds in ways that allow effective performance under a range of
conditions. But this general view is overly simple. The real world is very
complex and many factors influence nutritional responses in ways that we still
do not understand. New developments also arise that can markedly change
our nutritional thinking. Over the past 30 years I have found nutritional
research to be hugely absorbing and challenging, and I still find it so.
Diet accounts for about 70% of production costs. This is a fact repeated
regularly by nutritionists, only partly to emphasis their own importance.
Perhaps because of this, the nutritionist is often the first point of reference
when a problem of any sort arises, either to be blamed or to be expected to do
something about it. The problem may not always be overtly nutritional but
nutrition may influence it. Nutrition is thus one part, albeit an important one, of
the much larger production environment which can involve many other
disciplines.
As in commerce, so in research, the nutritionist can interact with many other
disciplines. True, some nutritionists have confined themselves to fairly narrow
fields during their careers but to me the excitement of research has involved
interacting with different subject areas and acquiring wider knowledge
and skills. I hope this will be apparent from the examples I shall give later.

Roslin Institute has a diagram of its research logic in which the core is
molecular and developmental biology, relating to a number of applications
including genetics, growth, reproduction and even welfare. Within this view the
subject of nutrition has been thought sometimes to sit rather uneasily and the
Institute has had difficulty incorporating nutrition within its scientific
strategy. This may in part reflect a failure by those most closely involved in
nutrition to make a convincing case for the importance of nutritional research
and knowledge. So I have drawn up an alternative diagram in which I see
nutrition as a core subject, relating to and integrating the effects of a very wide
range of other disciplines, as shown in Figure 1.
Genetics
In my diagram, I have placed the interaction with genetics prominently
because nutrition starts with the bird and geneticists create the bird. It has
been stated, usually by geneticists, that the role of nutrition is to allow the bird
to express its genetic potential. This is in large part true, though with some
exceptions. Over the years geneticists have improved the production potential
of birds so greatly that it has been a challenge to nutritionists to maintain
optimum nutrient supply. Of course, the task of the nutritionist has been
assisted by the presence of models that allow the prediction of the needs
for some of the main nutrients, given knowledge of genetic potential.
This of course, is part of the Morris philosophy but there are many examples of
where knowledge has been incomplete.
Life would undoubtedly be simpler if geneticists
Had been able to create perfect birds but so far they have not, and nutritionists
have often been called upon to overcome or alleviate some of the genetic
flaws. Broilers have had a history of metabolic weak- nesses, generally thought
to have arisen as a result of heavy selection pressure on the main economic
traits of growth and food efficiency. Leg weakness, ascites and some fatal
syndromes are all conditions where fast growth seems to have put pressure on
a range of metabolic systems often with disastrous consequences. In some
cases nutritionists have been able to identify specific nutritional factors that
can alleviate the problem in part or in whole.
But, where specific solutions have not been identified, the nutritionist has
often been able to help solve the problem at a more general level by slowing
growth to take the pressure off these vulnerable metabolic systems. This
slowing of growth, particularly during the early growing stage, has been
achieved by qualitative or quantitative nutrient restriction and has put the
nutritionist in the position of trying to limit the gains in potential achieved by
geneticists. Geneticists are now trying to avoid this conflict between nutrition
and genetics by breeding birds that have altered growth profiles that more
closely match those achieved by nutritional management. Of
course, as
the specific characteristics of different strains evolve either in response to
selection for different components of growth or to selection for particularly
beneficial metabolic characteristics (to counter specific weak- nesses), it will

be vital for nutritionists to identify optimum nutritional conditions for these

strains. In the short term, modelling may be less helpful in predicting these
new nutritional needs because the importance of nutrition genetic
interactions is likely to increase.
As a further example of the complementarity of genetics and nutrition, I would
like to cite the case of body composition. Body composition in broilers,
specifically the proportion of body fat, can be regulated nutritionally by
adjusting dietary protein: energy ratio. Increasing this ratio, within limits, will
decrease fatness and increase food efficiency with little effect on body weight.
The optimum ratio will depend upon the relative costs of energy and protein
and whether the bird is valued on the basis of body weight or meat content.
But fatness is also under genetic control, and it has proved possible to select
broilers that are genetically leaner. This has been achieved either by selecting
on the basis of sibling carcass analysis, as was carried out in France (Leclercq,
1988), Netherlands (Leenstra, 1988) and Israel (Cahaner, 1988).
An alternative approach (Whitehead and Griffin, 1982 ) involved selecting
on the basis of plasma concentration of very low density lipoprotein (VLDL).
The logic of this derives from the fact that most of the fat deposited in
adipose tissue in the chicken is synthesised in the liver and is then
transported by VLDL to the adipose tissue for deposition. Fat deposition is
thus largely proportional to the amount of VLDL in transit. Divergent selection
for high or low plasma VLDL concentration in fed birds was effective in
producing 2 lines with very different abdominal fat contents: a 2-and-a-halffold difference after 8 generations (Whitehead,
1990a).
It was then of interest to me as a nutritionist to compare genetic and nutritional
effects in these birds. In the case of our VLDL lines, we were able to show that
the responses of body fatness to dietary P/E were approximately parallel, as
shown in Figure 2. The birds here with 2% abdominal fat have very similar body
composition and weight in the 2 lines, with the genetic difference in fatness
being equivalent to a difference in dietary protein content of approximately 7%
(Whitehead, 1990b). As a long- term solution to the problem of excessive
fatness, genetics is obviously more efficient, though it takes time to achieve;
nutrition can be used as either a complementary or a short-term solution.

Molecular and cell biology

Some interesting interactions between nutrition and these subjects have been
discovered recently. Studies on bone biology have shown that tibial
dyschondro- plasia (TD) is a condition that can be influenced both by genetics

and nutrition. The basis for TD is a failure of cellular differentiation in the

growth plate. Chondrocytes start the transition from proliferation to
hypertrophy and mineralization but fail to complete this process. The result is a
build-up of prehypertrophic chondrocytes that constitutes the lesion and leads
to deformation of bone growth. At the genetic level, we have been trying to
identify candidate genes that might be involved in TD by regulating the
differentiation process.
Nutritional studies have already amply demonstrated that dietary
supplementation with vitamin D metabolites, particularly 1, 2 5dihydroxycholecalciferol (1,25-D ), can prevent TD (Edwards, 1990 ; Rennie et
al., 1993). We have devoted much effort to trying to establish the mechanism
by which 1, 25-D acts and have found that 1, 25-D can speed up the rate of
chondrocyte differentiation in vivo. Figure 3 shows the extent of differentiation
in slices through the normal growth plate, as measured by alkaline
phosphatase activity. There is no differentiation in the proliferative zone at the
top of the growth plate and no effect of dietary 1, 2 5- D o n t he
extent of terminal differentiation in the fully mature chondrocytes at the
bottom. However, in the prehypertrophic zone, differentiation is speeded up by
higher concentrations of 1,25-D in the diet (Farquharson et al.,1993).
1, 25-D is known to regulate the expression of a wide range of genes, including
its own receptor (VDR). Acting via the VDR, it also regulates genes for factors
known to control cell differentiation, including TGF-b and c-myc, both of
which are lacking in lesion cells (Loveridge et al., 1993). It is tempting to
speculate that TD involves a problem with a gene or genes regulating
chondrocyte development and that the nutritional effect of 1, 25-D is
associated with a direct effect on this gene or genes. Such a finding would
imply that the natural production of 1,25-D by metabolism of vitamin D in
broilers was inadequate and that normal genetic function benefited from
dietary supplementation with a novel type of nutrient.
This research is already having practical effects, in drawing attention to the
nutritional benefits of feeding vitamin D metabolites. 1,25-D is rather
expensive and somewhat toxic when supplied in moderate excess and is not
available commercially as a food additive at the moment. However, we
have found that another metabolite, 25-hydroxycholecalciferol (25-D ) is also
partially effective against TD, though at much higher dose rate, and not
always so consistently (Rennie and Whitehead, 1996). This compound is much
less toxic and also cheaper than 1, 25-D and is becoming avail- able
commercially. It may also offer the possibility of growth stimulation (Yarger et
al., 1995), in addition to TD prevention. More research is needed to identify the
optimum conditions for the use of 25-D but the use of vitamin D metabolites as
food additives is likely to become an interesting practical nutritional innovation.
I have given one example of an interrelation- ship between nutrition and
molecular biology which interests me but I do not think that nutritionists
need try to crave respectability for their science by seeking justification

through association with the increasingly dominant subject of molecular

biology purely for the sake of it. The use of molecular biological techniques
may at times be appropriate but need not be an end in themselves. It is
obvious that bodily development and metabolism depend fundamentally upon
both gene function and nutrient supply but many nutritional effects are already
sufficiently explicable in metabolic terms. For instance, where dietary effects
on fatness can be explained on the basis of the observed activities of
lipogenic enzymes that are of course gene products, it does not necessarily
increase nutritional knowledge greatly by confirming the predictable
changes in the expression of the genes for these enzymes. Though I do not
doubt that there will be benefits from a greater understanding of nutritional
regulation of gene expression, I think studies on inter me diary
metabolism will remain just as important in developing knowledge on
nutritional function.
Practical nutrition is also becoming a recipient of genetic and molecular
biological technology with the introduction of genetically improved foodstuffs.
High oil maize has already arrived and beans with higher protein and amino
acid contents are approaching. The main role for nutritionists has been to
evaluate these products but nutritionists can also provide advice on the most
appropriate characteristics to change. Changes in the content or availabilities
of amino acids, fatty acids, minerals or vitamins, incorporation of enzymes
improving digestive function and reductions in ant nutritive factors are all
possible and indeed, likely and will make life very interesting for nutritionists
and food formula- tors. They could also have an impact on the food supply
industry, on the market for synthetic nutrients and enzymes.
Biochemistry and pathology
For an example of interrelationships between nutrition, biochemistry and
pathology, I shall unashamedly stroll down memory lane. The story of Fatty
Liver and Kidney Syndrome (FLKS) has been history for more than 25 years but
it caught a few headlines in its day and the saga may be of interest to the
newer generation of poultry scientists.
FLKS started to become a problem in broiler production during the 1960s.
Birds at around 3 weeks of age would become unwilling or unable to walk and
would lie down and die within a few hours.
Mortality was variable, with usually a low background incidence of 0,5% to
1% but with occasional outbreaks where mortality could reach over 20%.
There were no indications the condition was infectious s but stress was
thought to be a precipitating factor. Often it was the largest birds that were
affected, so perhaps this was an early example of genetic selection for fast
growth predisposing birds to metabolic weakness.
Post mortem examination showed that the main abnormality was a paleness of
liver and kidney, caused by considerable accumulations of fat (Siller and Wight,
1975). However, this fat was brought about by infiltration rather than

degeneration and was not a likely cause of death; for instance, the fat did not
cause rupture of the liver and fatal hemorrhage, as in Fatty Liver Hemorrhagic
Syndrome (FLHS) in laying hens. The pathology in FLKS was thus unique and
did not resemble any reported nutritional deficiency conditions. However, diet
was perhaps involve d, because changing the food sometimes altered the
course of an outbreak.
Industry was concerned and came to our Institute (then the Poultry Research
Centre). The veterinarians were baffled and so turned to the nutritionists. We
set up a team comprising 2 pathologists, Walter Siller and the late Peter
Wight, 2 biochemists, Don Bannister and Tony Evans, and nutritionists Bob
Blair and myself. So we set off on a hunt for the cause of FLKS, not knowing in
which direction it would take us. Note that this initiative was taken by the
scientists themselves, not at the behest of Institute management, in the
inefficient days when scientists were allowed to do what they thought best,
before the Rothschild Report had such a dramatic effect on UK agricultural
research administration and funding. So it predated the time when policy
groups deliberated research priorities and required fully coasted proposals with
detailed procedures and milestones.
The first research priority was to be able to reproduce the condition in
sufficiently high incidence to study the effects of possible factors and to
provide enough material from affected but alive birds to carry out
metabolic studies. Anecdotal and some experimental evidence suggested that
FLKS was often associated with diets with high wheat content and could be
alleviated by increasing dietary protein and fat. A diet was formulated to have
a high content of ME and wheat but relatively low proportions of protein and fat
(Whitehead and Blair, 1974). This diet gave instant success and after some
refinements we had our killer diet which could reliably reproduce mortalities of
20% to 40%. This mortality was sufficiently high to study the effects of varying
different factors and gave the biochemists plenty of material to work with.
The initial nutritional studies confirmed a strong effect of dietary energy-toprotein ratio on mortality (Whitehead and Blair, 1974). As energy decreased or
protein content increased, mortality fell to low levels. At this point we had to
resist management pressure to the effect that since FLKS could largely be
prevented by feeding high protein diets, the problem could be considered
solved and research should be transferred to something more useful. But we
carried on, ruling out lipotropic agents, finding that stress or short periods of
fasting precipitated mortality and that providing ME in the form of fat rather
than carbohydrate reduced mortality. Was fatty acid composition important?
The answer was no, there was little difference between fats of very different
fatty acid composition. Then, a breakthrough: very low mortality when the killer
diet was supplemented with large quantities of vitamins (Whitehead et al.,
1975). But which was the important vitamin, or perhaps combination of
vitamins?

At this point, the biochemists provided important information on the

mechanism. They could relate the fatty infiltration in liver and kidneys to
mobilization of adipose tissue lipids but this appeared to be a secondary
rather than a primary effect. The most sinister change was in carbohydrate
rather than lipid metabolism, for the birds had very low blood glucose levels
and appeared to die from hypoglycemia. So, which vitamin was involved in
gluconeogenesis? Biotin was a prim e suspect (Bannister et al., 1975).
Yet another large-scale nutritional experiment was designed , in which the
killer diet was supplemented with vitamins, singly or in different
combinations, in a design that was optimized for biotin as well as for some
other vitamins. In the event, the answer was unequivocally that biotin alone
could prevent FLKS (Whitehead et al., 1976a).
Subsequently, we were able to explain the effects of FLKS in terms of glucose
supply and the partitioning of biotin between the 2 main enzymes for which it
is a co-factor, pyruvate carboxylase (PC), a gluconeogenic enzyme, and acetyl
coA carboxy- lase (ACC), a lipogenic enzyme. It appeared that ACC could
preferentially sequester biotin, so that when biotin supply was low and
lipogenic demand was high, as in a diet with low fat content and high energy:
protein ratio, lipogenesis was maintained but PC activity fell virtually to zero.
Despite this, birds were able to grow well, with their need for glucose being
met from the diet and also allowing breakdown of glycogen to supply short
term needs. However, if these birds were deprived of food or stress increased
glucose demand, or interrupted feeding reserves of glucose rapidly became
depleted and gluconeogenesis was inadequate to meet needs. A progressive
hypoglycemia ensued, leading to death. In response to these changes, adipose
tissue was mobilized and fat became infiltrated into liver, kidney and some
other tissues.
Why then, did FLKS occur on diets that were thought to contain a substantial
amount of biotin? It transpired that the biotin content of wheat-based diets was
inadequate because the natural biotin content of wheat is almost wholly
unavailable. Biotin was not included in commercial vitamin supple mints at that
time because it was expensive and a need for it had not been demonstrated.
The characteristic signs of biotin deficiency reported in the literature are poor
growth and skin and foot lesions. We confirmed these are the typical signs of
biotin deficiency when diets have good protein and fat content but when the fat
content is lower, skin lesions are less apparent and FLKS occurs (White- head et
al., 1976b). This then, is an unusual situation where the consequences of a
deficiency of one nutrient are highly dependent upon the balances between
other nutrients.
In retrospect, that research proved to be hugely cost-effective. It led to greatly
increased demand for biotin with the result that new manufacturing plants and
processes were developed and the price tumbled (or at least did not inflate so
much). Biotin deficiencies were looked for and found in other livestock species,
particularly pigs. I like to think of this project as a notable example of the

importance of multidisciplinary research and an indication of the strength of

relationships between nutrition, metabolism and pathology. I may have gone
back over 25 years to get this example but who is to say that current research
of this type, such as on the role of vitamin D metabolites in leg problems, will
not contribute to future revolutions in industrial practice?
Immunology
The impact of nutrition on health is not limited to deficiencies or syndromes;
modulation of the immune system by nutrients can influence the progression
of infectious diseases. Immunological impairment caused by nutrient
deficiency is, of course, well documented. However, immune stimulation by
nutrients has also been a subject of research and practical interest for some
time. Vitamins A and E, when fed at dietary concentrations consider- ably
above normal requirements, have been shown to increase antibody titers to
antigens and to decrease mortality in response to disease challenges (Tengerdy
and Nockels, 1975). These vitamins are antagonistic to each other and, with
limits to the use of vitamin A, it has been vitamin E that has been evaluated
more usually in commercial situations.
Field trials in both UK and USA have shown economic returns in broilers from
high-level dietary supplementation. In a large study in Northern Ireland,
McIlroy et al. (1993) reported a cost benefit from high level vitamin E
supplementation of broiler diets, in the presence of subclinical disease
challenge (infectious bursal disease, in that instance) and also in the
absence of subclinical disease.
Immunological interest is now extending to other vitamins as well as n-3 fatty
acids.
Immune stimulation may be an increasingly important objective in broiler
nutrition because continued selection in broilers is resulting in birds with less
efficient immune systems. However, immune stimulation has its
disadvantages also, because it involves a catabolic response that can result
in a transient growth depression. Is this another area of conflict between
geneticists and nutritionists, where geneticists breed faster growing birds with
impaired immune systems and nutritionists try to restore immune
responsiveness but at the expense of some growth? The interesting concept of
immune enhancement by injection of a nutrient into the egg during incubation
may be a way round this conflict (Gore and Qureshi, 1997).

Microbiology

The whole area of microbial control is becoming a hot topic in practical

nutrition as a result of the impending demise in the routine use of
antibiotics as growth promoters. Avoparcin has already been banned in

Europe and several other widely used antibiotics (including bacitracin,

virginiamycin and tylosin) are on the next list. Alternative approaches to growth
enhancement through microbial control are under intense scrutiny. Probiotics
have been around for some time as an alternative. In the role of competitive
exclusion of specific pathogens such as salmonella, bacterial infusions have
had some success but so far probiotics have not had a reputation for reliable
effectiveness as growth promoters. Perhaps continued research can
improve the effectiveness of this interesting concept. A possible interesting
development here is the discovery of a role for calcium phosphate in regulating
intestinal bacterial contents.
Newer methods of pathogen control involve the feeding of oligosaccharides
that inhibit the intestinal binding of some types of bacteria. Other food
treatments involve the use of organic acids or various heat treatment
technologies. The subject of the interaction of nutrition with micro-organisms,
in relation to immunological and intestinal function and the impacts on bird
health and performance and product quality is likely to expand considerably in
the coming years.

Environment

The nutrition of birds is influenced greatly by the environment in which they are
kept. Thermoregulation depends upon the balance between heat production by
the bird and heat loss to the environment. Thus environmental temperature
and humidity in lance energy utilization and food intake. Mathematical
models are available to predict optimum diet composition under a range
of environmental conditions but when these conditions become sufficiently
severe to result in stress, nutrition becomes more problematical. There are
established dietary modifications to help the bird cope with heat stress and to
minimize depressions in productivity. Some nutrients, particularly vitamins,
have anti-stress roles. Vitamin C is one well known example.
Vitamin E is another nutrient that has been found to have a role in heat stress.
Dietary supplementation with vitamin E can prevent some of the loss in egg
production by hens exposed to heat stress (Bollinger-Lee et al., 1998, 1999). A
rather novel mechanism is involved, relating to vitellogenin supply. Vitellogenin
is synthesised in the liver, under the control of estrogen which is synthesised in
the ovary. Vitellogenin is transported in the blood to the developing oocyte
where it is taken up as the major yolk protein precursor. It has been found that
plasma vitellogenin concentration was drastically reduced in heat stress and it
was hypothesized that this lack of yolk precursor was a major reason for the
depression in egg production. Feeding extra vitamin E partially restored
vitellogenin, as it did egg production. The various factors involved in
vitellogenin production were studied, from estrogen through to the formation of
vitellogenin mRNA which was taken as an indicator of vitellogenin synthesis.

Hepatic synthesis of Vg was lower in heat stress, but vitamin E did not appear
to affect synthesis because it had no effect on estrogen or on the amount of
vitellogenin mRNA.
Although stress thus depresses vitellogenin synthesis, we found, to our
surprise, that there was actually a n increase in the liver vitellogenin
concentration in stressed birds (Whitehead et al.,
1998). This could be explained by a decrease in Vg secretion from the liver,
which resulted in an increase in liver Vg content and a greatly decreased
plasma- to-liver ratio of vitellogenin. Provision of extra vitamin E permitted
better vitellogenin secretion and restored the ratio to more normal values.
There was a very close relationship at an individual bird level between the ratio
of plasma to liver vitellogenin and egg output.
The problem thus involves an inhibition of transport of vitellogenin out of the
liver that leads to a build-up in the liver, even though synthesis has been
depressed by heat stress. The cellular role by which vitamin E exerts this may
be related to the traditional anti-oxidant role of vita min E in maintaining
the normal membrane structure. Alternatively, there may be a novel
mechanism involving a specific role for vitamin E in membrane transport. This
is a very recently discovered example of the interaction of nutrition with
environment. There is currently considerable interest in the influence of other
nutrients on stress resistance.

Husbandry and economics

Within the overall context of husbandry, food management assumes great

importance in the effective commercial rearing of poultry, which is why
husbandry and economics have been combined in the same heading. With
food representing such a high proportion of production costs, efficient food
management is obviously of great economic importance. Modelling has
been of great assistance in this area. There are automated, computerized
systems for controlling how much food, of what composition, should be
provided to birds under controlled environmental conditions. Research on
choice feeding has shown the important extent to which birds can also
contribute to decision making. Food restriction, either quantitative or
qualitative, is also an important management tool for optimizing food
efficiency, health or body composition in broiler growing.
If efficient food management systems are important for broiler growing,
they are vital for broiler breeder performance. One of the major unsolved
problems in poultry production is the inverse relationship between growth and
reproductive performance. So the geneticists continue to compound the

problem by breeding a bird that in its freely expressed adult state is totally
unfit for life. If it does not fall off its legs, it is liable to die suddenly and
will have had great difficulty in reproducing itself. Again, it is left to the
nutritionist to try to solve the genetic problems. Severe food restriction helps
partially solve the egg production problem but leads to other dilemmas over
welfare. Important work on the physiology y of the female broiler breeder
(Hocking et al., 1987 ) has demonstrated the effect of food and
bodyweight restriction on minimizing multiple ovulation and also the stresses
involved. The challenge now needs to be taken up by physiologists and
geneticists, to identify the mechanisms interrelating growth and reproduction
and to breed a bird that will grow quickly yet be able to sustain
reproduction without the need for severe food or bodyweight restriction.

Behavior and welfare

Understand nag feeding behavior has been important in considering

nutrition in a wider context because, as has been pointed out before, chickens
have been poultry nutritionists long before man became interested in the
subject. It is not just the way the bird approaches its food in terms of pecking
responses to food form but also the way it responds to it. Complex feedback
mechanisms and satiety signals exist and have been exploited in the
exploration of choice feeding systems.
Of more specific interest in the welfare context has been the possibility of
modifying disadvantageous behaviors by nutrition. The example of tryptophan
is the most obvious. Tryptophan is a precursor for serotonin, a
neurotransmitting chemical, and dietary supplementation with tryptophan has
been shown to have a calming effect on chickens and to reduce feather
pecking (Shea ET al.1990).
Nutrition in a wider context has had a major impact on welfare, as apparent
from earlier sections of this talk. The prevention of deficiencies and
syndromes, such as FLKS by the formulation of balanced, nutritionally
adequate foods has obviously been important. Likewise, food management
system s for altering patterns of growth have contributed to the
alleviation of other problems, such as reducing mortality from ascites or
other causes or alleviating leg abnormalities.
Even when nutrition is not the principal factor in a problem, it is important to
get it right. One example is the avoidance of high dietary salt contents where
ascites is a problem. A more recent example is the case of osteoporosis and
bone fragility in laying hens. An industrial problem so, again, much of the
initial research is devoted to a nutritional solution. Our research has shown
how the bone loss in ageing hens is caused primarily by cellular factors

affecting bone remodeling, rather than by calcium deficiency (Rennie et

al., 1997). Nevertheless, it is important to avoid a calcium deficiency that
may make the problem worse. So the nutritional advice is: elevate dietary
calcium when hens are lit up, not at first egg; provide calcium in particulate
form; do not withdraw food a few days before depopulation.
These are nutritional tips for not making the problem worsebut the solutions
to osteoporosis lie in other directions. We have looked at genetic possibilities
and have been divergently selecting hens over a number of generations for
resistance or susceptibility to osteoporosis. The 6-fold reduction in humerus
fracture incidence under commercial breeding conditions is an indication of the
success of this approach (Bishop et al., 2000). However, effects of this
selection for bone quality are also becoming apparent in shell quality and it
is possible that new nutritional specifications will be needed for maximizing
both characteristics.
Nutrition
So far, and in keeping with my title, I have discussed the interrelationships
between nutrition and other disciplines. However, nutrition can also stand
alone as a subject. The high proportion of nutritional papers at poultry
science meetings testifies to the continuing importance of nutrition as a
research subject.
A dramatic stimulus to nutritional research has been provided in recent years
by the introduction of methods for modifying the nutritional value of foodstuffs.
This in turn has put a premium on the quantitative definition of foods. Routine
food evaluation may be a rather mundane activity but poultry nutrition is a
highly quantitative subject.
The description of energy has been subject that has produced its share of
controversy over the years. The debate over TME vs. AME produced a
considerable proportion of its own energy as heat, rather than light. The
general compromise has been that AME is used for formulation but TME is used
as a comparative means of evaluation, largely because of the practical
advantages of methods for TME measurement based on the Sibbald technique.
Alternative descriptions of energy, such as net energy and effective energy,
have their current proponents but seem to be failing to make headway in terms
of practical application.
The most important nutritional development in recent years has, of course,
been the introduction of food enzymes. These enzymes have increased
nutritional efficiency and altered the use of individual ingredients, such as
allowing an increase in the use of barley. They have been effective mainly in
allowing better digestion of conventional nutritional substances in foods,
rather than providing new sources of nourishment. Decreasing the viscosity of
intestinal contents has allowed more efficient digestion of nutrients, so ME
values and amino acid digestibilities are improved. The main enzymes are
carbohydrates but the more recent introduction of phytase has extended

interest to availability of phosphorus and other minerals involved in the phytate

complex. Quantification of the effects of enzymes on ME and amino acid
digestibility has become an important topic and contributions on enzymes
usually feature prominently as conference contributions. But I confess I enjoy
reports of investigations of enzyme mechanisms and novel applications rather
more than further confirmations that product X increases wheat ME by 3%.
Interest in the nature of intestinal contents, partly arising from studies on
enzyme mechanisms, has led to interesting findings on the effects of diet form
on nutritive value. The physical nature of food in terms of particle size, fine
or coarse mash vs. pellets, has been shown to affect endogenous enzyme
secretion and digestive efficiency (Nir, 1997). Wet feeding can also have some
interesting effects (Yasar and Forbes, 1999). These findings remind us that
standard food evaluation techniques may not always quantify accurately the
nutritive value of a diet.
The updating of requirements for modern genotypes remains important. There
have been important recent advances in the field of micronutrients, especially
vitamins, particularly in the light of NRC understating the requirements for
some vitamins. However, rather than just repeat require- mint studies under
ideal experimental conditions, I think it is important to carry out studies that
more closely represent the stressful conditions usually encountered in practice.
Our own research is identifying specific interactions between some vitamins
and heat or immunological stresses that should give a sounder basis for
practical vitamin supply.
Other micronutrients are also receiving attention. In the field of trace minerals,
interest is shifting to organic forms that seem to allow better absorption than
inorganic forms. These products could be helpful in resulting in less excretion of
potentially harmful elements. They could also open up new nutritional
opportunities. For instance, chromium in inorganic form is not usually
considered a useful dietary supplement but beneficial responses have been
reported to organic forms. Increased trace mineral utilization resulting from the
use of phytase is also worth investigation.
Is there a role for carnation, especially in all-vegetable diets? And what about
low molecular weight carbohydrates? I have already mentioned the use of
oligosaccharides to prevent intestinal bacterial binding. But direct nutritional
effects of other carbohydrates have been shown. For instance, xylitol can
increase calcium absorption and improve bone quality in rats (Attila et al.,
1998). Could it be helpful for bone or shell quality in poultry?
The impact of poultry nutrition on human nutrition and health should not be
ignored. After all, poultry products are produced for eating by humans and
provide rich and economic sources of protein and energy. They can also act as
specialty products. Eggs have been marketed in the past as alternative or
organic multivitamin supplements, though one would need to consume a fair
number to meet the recommended daily intake. Nonetheless, supplementation
of layers diets with vitamins or minerals such as selenium and zinc is still

promoted in developed and under developed parts of the world as a means of

promoting human health. The value of n-3 fatty acids in combating heart
disease is resulting in diets aimed at increasing the content of these fatty acids
in poultry meat products and eggs. In contrast, some poultry nutritional
practices seem to neglect human health implications. I refer to the
procedure advocated in some parts of the world of economizing on broiler
withdrawal diets by omitting the vitamin supple- mint. This can result in the
rapid depletion of vitamins from meat and is to be deplored.
The future
What does the future hold for poultry nutrition? I have seen tremendous
changes in the nutritional scene during my professional career and I have no
doubt that change will continue in many different areas. The enzyme
revolution will continue, with more enzymes designed to deal with different
structures. These enzymes will not only be aimed at improving the value of
nutrients but also inactivating ant nutrients. Genetic modification of foodstuffs
will also continue. Will cellulose become a digestible substance for poultry,
either by genetic modification of birds or plants or by the introduction of novel
food enzymes and/or processing methods?
A general benefit will arise from a greater understanding of nutritional
influences on immune function and the implications for growth or production.
The development of mathematical models to describe growth or production
requires predictability of response but in practice responses are influenced by
unpredictable stresses of disease or of environmental origin. The use of
nutraceuticals is likely to gather momentum. This will involve the feeding of
agents that have specific effects on digestive or metabolic systems, alter gut
micoflora and promote resistance to pathogens and/or stress. Antibiotics will
go, and I hope someone will be able to bring sense and predictability to the
probiotic field.
New nutritional substances or derivatives of existing ones are likely to be
introduced. My own
Interest in this area lies in vitamin D and its metabolites. In principle, the
benefits of feeding vitamin D metabolites to poultry are becoming apparent
and further research is likely to establish novel mechanisms of action. The
challenge now will be to develop products that are safe, effective and
economic. Of course, this raises the question of inclusion of vitamin D in
foods and legal limits. The current upper limits for vitamin D are not logical.
They are nowhere near values that have toxic implications for poultry or
consumers of poultry. Indeed, current health advice in human nutrition,
particularly for an increasingly aged population at risk from osteoporosis, is
aimed at increasing vitamin D intake. Benefits to both poultry and poultry
consumers arising from feeding higher levels to chickens deserve to be
explored.

Much of the point of my talk has been to document the importance of

interactions between nutrition and other disciplines. Nutritionists are often well
placed to advance reality in these relationships with other subjects because
they deal with whole animals rather than isolated biological systems and can
therefore give a holistic view. I have also detailed what I think is a particularly
strong relationship between nutrition and genetics.
Important future nutritional objectives will be to determine genetic influences
on nutrient use and define the nutritional conditions for new and altered
genotypes. There is already a renewed collaboration between the disciplines.
Fortunately, the days when the chief geneticist of an internationally renowned
breeding company could tell me that his company just fed the birds on chicken
feed are fast receding. But the interactions are not solely with genetics.
Nutrition interacts with so many disciplines, as I hope has become apparent in
this talk. It truly is the integrative science of my title. So, it seems especially
important to me that a genetically orientated Institute such as my own should
be more positive in integrating nutrition into its research strategy.
Finally, I leave you with my conclusion, namely that the continued health of
nutritional science and research is indispensable to the continued wellbeing of
poultry science and the poultry industry. I hope this will be reflected in research
funding.